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Hamartin is selectively induced by ischemia in hippocampal CA3 neurons and its ectopic expression at high level attenuates cellularproliferation. It also interacts with the ezrin-radixin-moesin family that activates the small GTP binding protein Rho to regulate cell adhesions.

Hamartin suppression increased locomotors activity and decreased habituation in a hippocampal-dependent task on the other hand overexpression in it will improved resistance to OGD through inducing productive autophagy by an mTORC1 dependent mechanism. Mutation of this gene implicated in corticaldysplasias associated to chronicepilepsy which exhibit a broad spectrum of structural changes resulted from alteration in proliferation, differentiation, migration and apoptosis of neural precursors during cortical development.